Variations in how much fluid is present in a person's thorax can take various forms and can have different causes. Eating salty foods can result in retaining excessive fluid in the thorax and elsewhere. Posture changes can also affect the amount of thoracic fluid. For example, moving from supine to standing can shift intravascular fluid away from the thorax toward the lower extremities.
Another example is pulmonary edema, which results in buildup of extravascular fluid in the lungs. In pulmonary edema, fluid accumulates in extracellular spaces, such as the spaces between lung tissue cells. One cause of pulmonary edema is congestive heart failure (CHF), which is also sometimes referred to as “chronic heart failure,” or as “heart failure.” CHF can be conceptualized as an enlarged weakened portion of heart muscle. The impaired heart muscle results in poor cardiac output of blood. As a result of such poor blood circulation, blood tends to pool in blood vessels in the lungs. This intravascular fluid buildup, in turn, results in the extravascular fluid buildup mentioned above. In sum, pulmonary edema can be one important condition associated with CHF.
Yet another example of thoracic fluid accumulation is pleural effusion, which is the buildup of extravascular fluid in the space between the lungs and the rib cage. Pleural effusion can also result from CHF because, as discussed above, intravascular fluid buildup can result in the extravascular interstitial fluid buildup. The extravascular fluid buildup of pulmonary edema can, in turn, result in the extravascular fluid buildup of pleural effusion.
CHF may also activate several physiological compensatory mechanisms. Such compensatory mechanisms are aimed at correcting the reduced cardiac output. For example, the heart muscle may stretch to increase its contractile power. Heart muscle mass may also increase. This is referred to as “hypertrophy.” The ventricle may also change its shape as another compensatory response. In another example, a neuro-endocrine response may provide an adrenergic increase in heart rate and contraction force. The Renin-Angiotensin-Aldosterone-System (RAAS) may be activated to induce vasoconstriction, fluid retention, and redistribution of blood flow. Although the neuro-endocrine response is compensatory, it may overload the cardiovascular system. This may result in myocardial damage, and may exacerbate CHF.
Diagnosing CHF may involve physical examination, electrocardiogram (ECG), blood tests, chest radiography, or echocardiography. Managing a CHF patient is challenging. CHF may require potent drugs. Moreover, treatment may be thwarted by the compensatory mechanisms, which may recompensate for the presence of the medical treatment. Therefore, treating CHF involves a delicate balance to properly manage the patient's hemodynamic status in a state of proper compensation to avoid further degeneration.
However, this delicate balance between compensation and effective CHF treatment is easily upset, even by seemingly benign factors, such as common medication (e.g., aspirin), physiological factors, excitement, or gradual progression of the disease. This may plunge the patient into a decompensation crisis, which requires immediate corrective action so as to prevent the deterioration of the patient's condition which, if left unchecked, can lead to death. In sum, accurately monitoring the symptoms of CHF, such as thoracic fluid accumulation, is very useful for avoiding such a decompensation crisis and properly managing the CHF patient in a state of relative well-being.